Presenilin-2 Mutation Causes Early Amyloid Accumulation and Memory Impairment in a Transgenic Mouse Model of Alzheimer's Disease
Figure 1
Early accumulation of amyloid deposition in the brains of PS2Tg2576 mice. Amyloid plaques were immunoreacted with the 82E1 monoclonal antibody against the N-terminal of Aβ. (a) At 2-3 months of age, typical amyloid plaques were positively detected in PS2Tg2576 mouse brains. (b) At 4-5 months, amyloid depositions were significantly observed in the hippocampus and the cerebral neocortex of the PS2Tg2576 mice. (c) In the 6-7 month-old PS2Tg2576 mice, markedly high levels of typical amyloid plaques were observed. (d) No plaques were detected in the brains of the Tg2576 mice at 6-7-months of age. The insets show a high magnification image of the boxed area. The arrowheads indicate plaques in the PS2Tg2576 mice at 2-3 months of age. The scale bars represent 200 μm and 5 μm in the main panel and inset, respectively.